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Exp Ther Med. 2016 Dec;12(6):4175-4181. doi: 10.3892/etm.2016.3903. Epub 2016 Nov 15.

Sesamin attenuates allergic airway inflammation through the suppression of nuclear factor-kappa B activation.

Author information

1
Department of Anatomy, Histology and Embryology, Yanbian University Medical College, Yanji, Jilin 133002, P.R. China.
2
Department of Respiratory Medicine, Yanbian University, Yanji, Jilin 133000, P.R. China.
3
Department of Respiratory Medicine, College of Pharmacy, Yanbian University, Yanji, Jilin 133002, P.R. China.

Abstract

The aim of the present study is to determine the role of sesamin, the most abundant lignan in sesame seed oil, on the regulation of allergic airway inflammation in a murine asthma model. A BALB/c mouse model with allergic asthma was used to evaluate the effects of sesamin on nuclear factor-kappa B (NF-κB) activation. An enzyme-linked immunosorbent assay was used to determine protein expression in bronchoalveolar lavage (BAL) fluids. Hematoxylin and eosin staining was performed to examine histological changes. Moreover, western blot analysis was used to detect the expression of proteins in tissues. Prior to administering sesamin, the mice developed the following pathophysiological features of asthma: An increase in the number of inflammatory cells, increased levels of interleukin (IL)-4, IL-5 and IL-13, decreased levels of interferon-γ in BAL fluids and lung tissues, increased immunoglobulin E (IgE) levels in the serum and an increased activation of NF-κB in lung tissues. Following treatment with sesamin, the mice had evidently reduced peribronchiolar inflammation and airway inflammatory cell recruitment, inhibited production of several cytokines in BAL fluids and lung tissues, and decreased IgE levels. Following inhalation of ovalbumin, the administration of sesamin also inhibited the activation of NF-κB. In addition, sesamin administration reduced the phosphorylation of p38 mitogen-activated protein kinases (MAPKs). The present study demonstrates that sesamin decreases the activation of NF-κB in order to attenuate allergic airway inflammation in a murine model of asthma, possibly via the regulation of phosphorylation of p38 MAPK. These observations provide an important molecular mechanism for the potential use of sesamin in preventing and/or treating asthma, as well as other airway inflammatory disorders.

KEYWORDS:

Th2 cytokine; airway inflammation; asthma; nuclear factor-kappa B; sesamin

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